FB2025_01 , released February 20, 2025
Allele: Dmel\sdtEH681
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General Information
Symbol
Dmel\sdtEH681
Species
D. melanogaster
Name
FlyBase ID
FBal0032675
Feature type
allele
Associated gene
Dmel\sdt
Associated Insertion(s)
Carried in Construct
Also Known As
sdtEH
Key Links
Genomic Maps

Allele class

amorphic allele - genetic evidence

Mutagen
Nature of the Allele
Allele class

amorphic allele - genetic evidence

(Tepass and Knust, 1993)
Mutagen
ethyl methanesulfonate
(Eberl and Hilliker, 1988)
Progenitor genotype
Cytology
Description

Nucleotide substitution: C?T.

(Hong et al., 2001)

Amino acid replacement: Q156term.

(Hong et al., 2001)
Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
point_mutation
X:8,225,124..8,225,124 [+]
Nucleotide change:

C8225124T

Reported nucleotide change:

C?T

Amino acid change:

Q156term | sdt-PB; Q231term | sdt-PE; Q884term | sdt-PG; Q133term | sdt-PI; Q372term | sdt-PJ; Q786term | sdt-PL; Q884term | sdt-PM; Q156term | sdt-PN; Q470term | sdt-PO

Reported amino acid change:

Q156term

(Hong et al., 2001)
Variant Molecular Consequences
Associated Sequence Data
DDBJ / EMBL / GenBank
DNA sequence
Protein sequence
 
UniProtKB/Swiss-Prot
    UniProtKB/TrEMBL
      Expression Data
      Reporter Expression
      Additional Information
      Statement
      Reference
       
      Marker for
      Reflects expression of
      Reporter construct used in assay
      Human Disease Associations
      Disease Ontology (DO) Annotations
      Models Based on Experimental Evidence ( 0 )
      Disease
      Evidence
      References
      Modifiers Based on Experimental Evidence ( 0 )
      Disease
      Interaction
      References
      Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
       
      Disease-implicated variant(s)
       
      Phenotypic Data
      Phenotypic Class
      Phenotype Manifest In
      Detailed Description
      Statement
      Reference

      Homozygous clones in the wing disc survive and do not show polarity defects.

      (Padash Barmchi et al., 2016)

      sdtEH681 follicle cell clones, induced by driving Scer\FLP1Scer\UAS.cUa under the control of the Scer\GAL4e22c driver, are morphologically indistinguishable from wild type.

      sdtEH681 embryos show reduced cuticle production, typically resulting in embryos with fragmented cuticle.

      (Horne-Badovinac and Bilder, 2008)

      Homozygous eye clones have no obvious effects on photoreceptor cell morphogenesis. No light-induced retinal degeneration is seen.

      (Berger et al., 2007)

      Epithelial cells of ectodermal origin lose their apicobasal polarity resulting in the loss of epithelial integrity and cell death. Both epidermal and amnioserosa cells of stage 10 lack zonula adherens junctions (ZA) and the number of spot adherens junctions (SAJ) is lower. The structure of all ectodermally derived epithelia is affected to varying extents.

      (Grawe et al., 1996)

      First defects in zonula adherens formation are seen at the onset of germband extension on the dorsal side of the embryo in the developing amnioserosa. The distribution of adherens junction material at the apicolateral boundary is more irregular.

      (Tepass, 1996)

      Cell death is dramatically increased. Although no extra mesoderm cells are induced to become hemocytes the macrophages become larger than average. Cellular debris becomes located extracellularly in the hemolymph.

      (Tepass et al., 1994)

      At stage 11 of embryogenesis ectodermal cells lose their normal columnar shape and round up. 1-2hr later cells form clusters, rather than a monolayer. Dead cells are often seen on the outside of the embryo. Vesicles form of cells retaining epithelial characteristics, and later secrete grains or vesicles of cuticle. Many cells fail to become integrated into an epithelial sheet. Degeneration is most extreme in the epidermis, the pharynx and the amnioserosa, and least extreme in the proventriculus and Malpighian tubules which develop almost normally.

      (Tepass and Knust, 1993)

      Aberrant organogenesis and small shreds of cuticle.

      (Eberl and Hilliker, 1988)
      External Data
      Interactions
      Show genetic interaction network for Enhancers & Suppressors
      Phenotypic Class
      Enhancer of
      Statement
      Reference

      sdtEH681 is an enhancer of visible phenotype of Scer\GAL4en-e16E, armUAS.cWa

      (Greaves et al., 1999)
      Suppressor of
      Statement
      Reference

      sdtEH681 is a suppressor of visible phenotype of Scer\GAL4en-e16E, shgi.UAS.Tag:SS(aos),Tag:MYC

      (Greaves et al., 1999)
      Phenotype Manifest In
      Additional Comments
      Genetic Interactions
      Statement
      Reference
      Xenogenetic Interactions
      Statement
      Reference
      Complementation and Rescue Data
      Fails to complement

      sdtE195

      (Berger et al., 2007)

      sdtK85

      (Berger et al., 2007)

      sdtK70

      (Berger et al., 2007)

      sdtXN

      (Berger et al., 2007)

      sdtM120

      (Berger et al., 2007)

      sdtXH21

      (Berger et al., 2007)

      sdt7D

      (Berger et al., 2007)

      sdtXP

      (Berger et al., 2007)
      Partially rescued by

      sdtEH681 is partially rescued by Scer\GAL4nanos.PG/sdtB.UAS

      (Horne-Badovinac and Bilder, 2008)

      sdtEH681 is partially rescued by sdtA.UAS/Scer\GAL4nanos.PG

      (Horne-Badovinac and Bilder, 2008)

      sdtEH681 is partially rescued by Scer\GAL4da.G32/sdtUAS.MAGUK

      (Bachmann et al., 2001)
      Comments

      Expression of sdtA.Scer\UAS under the control of the maternal driver Scer\GAL4nos.PG partially rescues the cuticle phenotype seen in sdtEH681 mutant embryos. 43% of embryos examined showed continuous cuticle over 2/3 of the surface compared to 8% in the negative control.

      Expression of sdtB.Scer\UAS under the control of the maternal driver Scer\GAL4nos.PG partially rescues the cuticle phenotype seen in sdtEH681 mutant embryos. 13% of embryos examined showed continuous cuticle over 2/3 of the surface compared to 8% in the negative control and approximately 10% only displayed fragments of cuticle compared to over 70% in controls.

      (Horne-Badovinac and Bilder, 2008)
      Images (0)
      Mutant
      Wild-type
      Stocks (1)
      Notes on Origin
      Discoverer
      Comments
      Comments

      sdtEH681, sdt7D, sdt2, sdt3, sdtK8 and Df(1)HA11 all have a similar phenotype. The sdt mutant phenotype is not enhanced by deleting the sdt gene from the maternal germline. The phenotype of amorphic sdt mutants is essentially the same as the phenotype of amorphic crb mutants. Embryos doubly mutant for sdt and crb mutants show the same phenotype as embryos singly mutant for either gene. Phenotype is unaffected by a duplication for crb+, Dp(3;3)M95A+13.

      (Tepass and Knust, 1993)
      External Crossreferences and Linkouts ( 0 )
      Synonyms and Secondary IDs (3)
      References (15)